Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SHOCK”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2003

Altered temporal profile of heat shock factor 1 phosphorylation and heat shock protein 70 expression induced by heat shock in nucleus tractus solitarii of spontaneously hypertensive rats.

BACKGROUND: We demonstrated recently that heat shock (HS)-induced heat shock protein 70 (HSP70) expression in bilateral nucleus tractus solitarii (NTS), the terminal site in the brain stem for primary baroreceptor afferents, confers cardiovascular protection against heatstroke by potentiating baroreceptor reflex (BRR) response. This study evaluated the hypothesis that altered regulation of HSP70 expression may be associated with the heightened susceptibility to heatstroke during hypertension. METHODS AND RESULTS: Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats anesthetized with propofol were used. Compared with WKY rats, significant induction in HSP70 or phosphorylation of heat shock factor 1 (HSF1), but not HSF2, in the NTS and potentiation of BRR response in SHR occurred earlier (4 versus 8 hours), reaching peak magnitude sooner (16 versus 24 hours), and declined more rapidly after a brief hyperthermic HS (42+/-0.5 degrees C for 15 minutes). The protection conferred by HS against hypotension and bradycardia during the onset of heatstroke (45 degrees C for 60 minutes), although effective, was less effective in SHR. Microinjection bilaterally into the NTS of the selective protein kinase A (PKA) inhibitor H-89 (100 pmol) or the selective PKC inhibitor calphostin C (100 pmol) significantly attenuated all of the above events induced in SHR by HS. However, only H-89 was effective in WKY rats. CONCLUSIONS: An altered temporal profile of HS-induced HSP70 expression or potentiation of BRR response by concurrent activation via both PKA and PKC pathways of phosphorylation of HSF1 in the NTS may be associated with greater susceptibility to heatstroke during hypertension.

Animals↗
PubMed2002

Induction of heat shock protein 47 synthesis by TGF-beta and IL-1 beta via enhancement of the heat shock element binding activity of heat shock transcription factor 1.

With most immunological reactions, tissue fibrosis, collagen overproduction caused by immune cytokines, is inevitably associated. Among the various immune cytokines, heat shock protein 47 (HSP47) is a procollagen-specific molecular chaperon and is essential for secretion of procollagen from cells. Induction of HSP47 by TGF-beta has been previously reported in rat skeletal myoblasts and mouse osteoblasts, but not in human diploid fibroblasts. As for IL-1beta, its effect on HSP47 has not been elucidated. In the present study, using human embryonic lung fibroblast cells, we first disclosed that both TGF-beta and IL-1beta induced HSP47 synthesis. We then revealed that the binding of the heat shock element (HSE) by heat shock transcription factor 1 (HSF1) was enhanced by both cytokines. We further demonstrated that trimer formation of HSF1, which is essential for its binding to HSE, was induced by these cytokines. The enhancement of HSP47 synthesis and their trimer formation of HSF1 were augmented by using a combination of both cytokines. Collectively, TGF- beta and IL-1beta were found to induce trimer formation of HSF1 which in turn bound to HSE of HSP47, resulting in the enhancement of HSP47 expression. Thus, HSP47 could well be a good candidate for molecular targeting in controlling tissue fibrosis, given that both principal fibrinogenetic cytokines (TGF-beta, IL-1beta) are commonly involved in its induction through HSF1 trimerization.

Cell Line↗
PubMed1989

Characterization of the heat shock response in cultured sugarcane cells : I. Physiology of the heat shock response and heat shock protein synthesis.

Effect of heat shock on the growth of cultured sugarcane cells (Saccharum officinarum L.) was measured. Heat shock (HS) treatment at 36 to 38 degrees C (2 hours) induced the development of maximum thermotolerance to otherwise nonpermissive heat stress at 54 degrees C (7 minutes). Optimum thermotolerance was observed 8 hours after heat shock. Development of thermotolerance was initiated by treatments as short as 30 minutes at 36 degrees C. Temperatures below 36 degrees C or above 40 degrees C failed to induce maximum thermotolerance. In vivo labeling revealed that HS at 32 to 34 degrees C induced several high molecular mass heat shock proteins (HSPs). A complex of 18 kilodalton HSPs required at least 36 degrees C treatment for induction. The majority of the HSPs began to accumulate within 10 minutes, whereas the synthesis of low molecular mass peptides in the 18 kilodalton range became evident 30 minutes after initiation of HS. HS above 38 degrees C resulted in progressively decreased HSP synthesis with inhibition first observed for HSPs larger than 50 kilodaltons. Analysis of two-dimensional gels revealed a complex pattern of label incorporation including the synthesis of four major HSPs in the 18 kilodalton range and continued synthesis of constitutive proteins during HS.

Journal Article↗
PubMed1991

Expression of heat shock protein 70 and heat shock cognate 70 messenger RNAs in rat cortex and cerebellum after heat shock or amphetamine treatment.

The expression of strictly inducible hsp70 mRNAs and constitutively expressed hsc70 mRNAs was compared in cerebellum and cerebral cortex of control rats, heat-shocked rats, and rats made hyperthermic with amphetamine. An hsc70-specific oligonucleotide probe identified a 2.55-kb mRNA in cerebellum and cerebral cortex of all rats. An hsp70-specific oligonucleotide probe identified a 3.05-kb mRNA and a 3.53-kb mRNA in cerebellum and cerebral cortex of heat-shocked and amphetamine-treated rats, but not in control rats. Quantitation demonstrated that both hsp70 and hsc70 mRNA levels, relative to 18S rRNA levels, were increased following each treatment. The relative levels of both mRNAs were higher in cerebellum than in cerebral cortex. In amphetamine-treated rats, hsc70 mRNA relative levels increased at body temperatures greater than 39 degrees C, whereas hsp70 mRNA synthesis was induced at temperatures greater than 40 degrees C. Total thermal response values and relative levels of both mRNAs were compared. The results suggested that both the transcription and turnover of hsp70 mRNAs differed between cerebellum and cerebral cortex. At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.

Amphetamine↗
PubMed2006

Heat shock protein 25 or inducible heat shock protein 70 activates heat shock factor 1: dephosphorylation on serine 307 through inhibition of ERK1/2 phosphorylation.

The expression of heat shock proteins (HSPs) is known to be increased via activation of heat shock factor 1 (HSF1), and excess expression of HSPs exerts feedback inhibition of HSF1. However, the molecular mechanism to modulate such relationships between HSPs and HSF1 is not clear. In the present study, we show that stable transfection of either Hsp25 or inducible Hsp70 (Hsp70i) increased expression of endogenous HSPs such as HSP25 and HSP70i through HSF1 activation. However, these phenomena were abolished when the dominant negative Hsf1 mutant was transfected to HSP25 or HSP70i overexpressed cells. Moreover, the increased HSF1 activity by either HSP25 or HSP70i was found to result from dephosphorylation of HSF1 on serine 307 that increased the stability of HSF1. Either HSP25 or HSP70i inhibited ERK1/2 phosphorylation because of increased MKP1 phosphorylation by direct interaction of these HSPs with MKP1. Treatment of HOS and NCI-H358 cells, which showed high expressions of endogenous HSF1, with small interfering RNA (siRNA) of either HSP27 (siHSP27)or HSP70i (siHSP70i) inhibited both HSP27 and HSP70i proteins; this was because of increased ERK1/2 phosphorylation and serine phosphorylation of HSF1. The results, therefore, suggested that when the HSF1 protein level was high in cancer cells, excess expression of HSP27 or HSP70i strongly facilitates the expression of HSP proteins through HSF1 activation, resulting in severe radio- or chemoresistance.

Animals↗
PubMed2000

Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

OBJECTIVES: We sought to delineate the angiographic findings, clinical correlates and in-hospital outcomes in patients with cardiogenic shock (CS) complicating acute myocardial infarction. BACKGROUND: Patients with CS complicating acute myocardial infarction carry a grave prognosis. Detailed angiographic findings in a large, prospectively identified cohort of patients with CS are currently lacking. METHODS: We compared the clinical characteristics, angiographic findings, and in-hospital outcomes of 717 patients selected to undergo angiography and 442 not selected, overall and by shock etiology: left or right ventricular failure versus mechanical complications. RESULTS: Patients who underwent angiography had lower baseline risk and a better hemodynamic profile than those who did not. Overall, 15.5% of the patients had significant left main lesions on angiography, and 53.4% had three-vessel disease, with higher rates of both for those with ventricular failure, compared with patients who had mechanical complications. Among patients who underwent angiography, those with ventricular failure had significantly lower in-hospital mortality than patients with mechanical complications (45.2% vs. 57.0%; p = 0.021). Importantly, for patients with ventricular failure, in-hospital mortality also correlated with disease severity: 35.0% for no or single-vessel disease versus 50.8% for three-vessel disease. Furthermore, mortality was associated with the culprit lesion location (78.6% in left main lesion, 69.7% in saphenous vein graft lesions, 42.4% in circumflex lesions, 42.3% in left anterior descending lesions, and 37.4% in right coronary artery lesions), and Thrombolysis In Myocardial Infarction (TIMI) flow grade (46.5% in TIMI 0/1, 49.4% in TIMI 2 and 26% in TIMI 3). CONCLUSIONS: Patients who underwent angiographic study in the SHOCK Trial Registry had a more benign cardiac risk profile, more favorable hemodynamic findings and lower in-hospital mortality than those for whom angiograms were not obtained. Patients with CS caused by ventricular failure had more severe atherosclerosis, and a different distribution of culprit vessel involvement but lower in-hospital mortality, than those with mechanical complications. Overall in-hospital survival correlates with the extent of coronary artery obstructions, location of culprit lesion and baseline coronary TIMI flow grade.

Aged↗
PubMed2000

The clinical profile of patients with suspected cardiogenic shock due to predominant left ventricular failure: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?

OBJECTIVES: We sought to evaluate the frequency of pulmonary congestion and associated clinical and hemodynamic findings in patients with suspected cardiogenic shock (CS). BACKGROUND: The prevalence of pulmonary congestion in the setting of CS is uncertain. METHODS: The 571 SHOCK Trial Registry patients with predominant left ventricular failure (LVF) were divided into four groups: Group A = no pulmonary congestion/no hypoperfusion = 14 (3%), Group B = isolated pulmonary congestion = 32 (6%), Group C = isolated hypoperfusion = 158 (28%) and Group D = congestion with hypoperfusion = 367 (64%). Statistical comparisons between Group C and D only, with regard to patient demographics, hemodynamics, treatment and outcome, were made. RESULTS: A significant proportion of patients with shock had no pulmonary congestion (Group C = 28%, 95% CI, 24% to 31%). Age and gender in this group were similar to Group D. Group C patients were less likely to have a prior MI (p = 0.028), congestive heart failure (p = 0.005) and renal insufficiency (p = 0.032), and the index MI was less likely to be anterior (p = 0.044). Cardiac output, cardiac index and ejection fraction were similar for the two groups but pulmonary capillary wedge pressure was slightly lower for Group C (22 vs. 24 mm Hg, p = 0.012). Treatment with thrombolysis, angioplasty and bypass surgery was similar in the two groups. In-hospital mortality rates for Groups C and D were 70% and 60%, respectively (p = 0.036). After adjustment, this difference was no longer statistically significant (p = 0.153). CONCLUSIONS: Absence of pulmonary congestion at initial clinical evaluation does not exclude a diagnosis of CS due to predominant LVF and is not associated with a better prognosis.

Aged↗
PubMed2000

Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

OBJECTIVES: We sought to investigate the potential benefit of thrombolytic therapy (TT) and intra-aortic balloon pump counterpulsation (IABP) on in-hospital mortality rates of patients enrolled in a prospective, multi-center Registry of acute myocardial infarction (MI) complicated by cardiogenic shock (CS). BACKGROUND: Retrospective studies suggest that patients suffering from CS due to MI have lower in-hospital mortality rates when IABP support is added to TT. This hypothesis has not heretofore been examined prospectively in a study devoted to CS. METHODS: Of 1,190 patients enrolled at 36 participating centers, 884 patients had CS due to predominant left ventricular (LV) failure. Excluding 26 patients with IABP placed prior to shock onset and 2 patients with incomplete data, 856 patients were evaluated regarding TT and IABP utilization. Treatments, selected by local physicians, fell into four categories: no TT, no IABP (33%; n = 285); IABP only (33%; n = 279); TT only (15%; n = 132); and TT and IABP (19%; n = 160). RESULTS: Patients in CS treated with TT had a lower in-hospital mortality than those who did not receive TT (54% vs. 64%, p = 0.005), and those selected for IABP had a lower in-hospital mortality than those who did not receive IABP (50% vs. 72%, p < 0.0001). Furthermore, there was a significant difference in in-hospital mortality among the four treatment groups: TT + IABP (47%), IABP only (52%), TT only (63%), no TT, no IABP (77%) (p < 0.0001). Patients receiving early IABP (< or = 6 h after thrombolytic therapy, n = 72) had in-hospital mortality similar to those with late IABP (53% vs. 41%, n = 64, respectively, p = 0.172). Revascularization rates differed among the four groups: no TT, no IABP (18%); IABP only (70%); TT only (20%); TT and IABP (68%, p < 0.0001); this influenced in-hospital mortality significantly (39% with revascularization vs. 78% without revascularization, p < 0.0001). CONCLUSIONS: Treatment of patients in cardiogenic shock due to predominant LV failure with TT, IABP and revascularization by PTCA/CABG was associated with lower in-hospital mortality rates than standard medical therapy in this Registry. For hospitals without revascularization capability, a strategy of early TT and IABP followed by immediate transfer for PTCA or CABG may be appropriate. However, selection bias is evident and further investigation is required.

Aged↗
PubMed2000

Diabetes mellitus in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

OBJECTIVES: We sought to examine the role of diabetes mellitus in cardiogenic shock (CS) complicating acute myocardial infarction (AMI) in the SHOCK Trial Registry. BACKGROUND: The characteristics, outcomes and optimal treatment of diabetic patients with CS complicating AMI have not been well described. METHODS: Baseline characteristics, clinical and hemodynamic measures, treatment variables, shock etiologies and comorbid conditions were compared for 379 diabetic and 784 nondiabetic patients. Logistic regression was used to examine the association between diabetes and in-hospital mortality, after adjustment for baseline differences. RESULTS: Diabetics were less likely than nondiabetics to undergo thrombolysis (28% vs. 37%; p = 0.002) or attempted revascularization (40% vs. 49%; p = 0.008). The survival benefit for diabetics selected for percutaneous or surgical revascularization (55% vs. 19% without revascularization) was similar to that for nondiabetics (59% vs. 25%). Overall unadjusted in-hospital mortality was significantly higher for diabetics (67% vs. 58%; p = 0.007), but diabetes was only a borderline predictor of mortality after adjustment for baseline and treatment differences (odds ratio for death, 1.36; 95% confidence interval, 1.00 to 1.84; p = 0.051). CONCLUSIONS: Diabetics with CS complicating AMI have a higher-risk profile at baseline, but after adjustment, diabetics have an in-hospital survival rate that is only marginally lower than that of nondiabetics. Diabetics who undergo revascularization derive a survival benefit similar to that of nondiabetics.

Aged↗
PubMed2004

A Trypanosoma cruzi heat shock protein 40 is able to stimulate the adenosine triphosphate hydrolysis activity of heat shock protein 70 and can substitute for a yeast heat shock protein 40.

The process of assisted protein folding, characteristic of members of the heat shock protein 70 (Hsp70) and heat shock protein 40 (Hsp40) molecular chaperone families, is important for maintaining the structural integrity of cellular protein machinery under normal and stressful conditions. Hsp70 and Hsp40 cooperate to bind non-native protein conformations in a process of adenosine triphosphate (ATP)-regulated assisted protein folding. We have analysed the molecular chaperone activity of the cytoplasmic inducible Hsp70 from Trypanosoma cruzi (TcHsp70) and its interactions with its potential partner Hsp40s (T. cruzi DnaJ protein 1 [Tcj1] and T. cruzi DnaJ protein 2 [Tcj2]). Histidine-tagged TcHsp70 (His-TcHsp70), Tcj1 (Tcj1-His) and Tcj2 (His-Tcj2) were over-produced in Escherichia coli and purified by nickel affinity chromatography. The in vitro basal specific ATP hydrolysis activity (ATPase activity) of His-TcHsp70 was determined as 40 nmol phosphate/min/mg protein, significantly higher than that reported for other Hsp70s. The basal specific ATPase activity was stimulated to a maximal level of 60 nmol phosphate/min/mg protein in the presence of His-Tcj2 and a model substrate, reduced carboxymethylated alpha-lactalbumin. In vivo complementation assays showed that Tcj2 was able to overcome the temperature sensitivity of the ydj1 mutant Saccharomyces cerevisiae strain JJ160, suggesting that Tcj2 may be functionally equivalent to the yeast Hsp40 homologue (yeast DnaJ protein 1, Ydj1). These data suggest that Tcj2 is involved in cytoprotection in a similar fashion to Ydj1, and that TcHsp70 and Tcj2 may interact in a nucleotide-regulated process of chaperone-assisted protein folding.

Adenosine Triphosphatases↗
PubMed2005

Mechanism of cardioprotection following trauma-hemorrhagic shock by a selective estrogen receptor-beta agonist: up-regulation of cardiac heat shock factor-1 and heat shock proteins.

Although 17beta-estradiol (E2) administration following trauma-hemorrhage (T-H) improves cardiac function in male rodents, it is not known whether the salutary effects of E2 are mediated via estrogen receptor (ER)-alpha or ER-beta, and whether cardiac heat shock proteins (Hsp) are affected by E2 administration. Male Sprague-Dawley rats underwent T-H (mean BP 40 mmHg for 90 min, then resuscitation). ER-alpha agonist propyl pyrazole triol (PPT) (5 microg/kg), ER-beta agonist diarylpropiolnitrile (DPN) (5 microg/kg), or vehicle (10% DMSO) was injected subcutaneously during resuscitation. At 24 h after T-H or sham operation, cardiac output (CO), stroke volume (SV), mean blood pressure, and +/- dP/dt max were measured (n=6 rats per group). Cardiac Hsp32, 60, 70, and 90 mRNA/protein expressions and heat shock factor (HSF)-1 DNA binding activity were determined. One-way ANOVA and Tukey's test were used for statistical analysis. CO, SV and +/- dP/dt(max) decreased significantly after T-H, however, administration of ER-beta agonist DPN after T-H restored the above parameters. Moreover, DPN treatment prevented T-H-mediated decrease in Hsp60 mRNA/protein and Hsp90 protein expressions in the heart. Hsp32 and Hsp70 mRNA/protein expression and HSF-1 DNA binding activity in the hearts were increased even above the shams in DPN treated T-H rats. In contrast, no significant change in the above parameters was observed in T-H rats treated with ER-alpha agonist PPT. Thus, the salutary effects of E2 on cardiac function are mediated via ER-beta and ER-beta-induced up-regulation of Hsp likely plays a significant role in the E2-mediated cardioprotection after T-H.

Animals↗
PubMed2006

Interhospital transfer for early revascularization in patients with ST-elevation myocardial infarction complicated by cardiogenic shock--a report from the SHould we revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) trial and registry.

BACKGROUND: Early revascularization (ERV) in patients with ST-elevation myocardial infarction (STEMI) and cardiogenic shock (CS) reduces mortality rates. Patients admitted to hospitals without revascularization capability have high mortality rates and are not often transferred for ERV. METHODS: Transfer and direct-admit patients with STEMI from the SHOCK Trial and Registry with left ventricular failure (N = 969) were analyzed to determine benefit of ERV in transfer patients. RESULTS: Transfer patients (46%) were younger and less likely to have prior hypertension, myocardial infarction, and heart failure. They received more aggressive treatment, were revascularized later after CS (median 7.3 vs 3.9 hours, P = .0002), and had similar adjusted inhospital mortality compared with direct-admit patients (55% vs 56%). Inhospital mortality was lower in ERV than no/late revascularization (41% vs 53%, P = .017 for transfer patients; 55% vs 71%, P = .0003 for direct-admit patients). Multiple logistic regression showed that inhospital mortality was associated with age (odds ratio [OR] 1.50 per decade increase, 95% CI 1.31-1.73, P < .0001), mean arterial pressure (OR 0.98 per 1 mm Hg increase, 95% CI 0.97-0.99, P < .0001), fibrinolysis before CS (OR 0.65, 95% CI 0.52-0.96, P = .040), and ERV (OR 0.70, 95% CI 0.52-0.96, P = .028), but not transfer admission (OR 1.23, 95% CI 0.86-1.74, P = .26). CONCLUSIONS: Despite longer time to treatment, transfer patients are a selected population with similar adjusted inhospital mortality and ERV benefit as direct-admit patients. Selected patients with STEMI and CS admitted to hospitals without revascularization capability should be transferred to centers with revascularization capability for immediate angiography.

Aged↗
PubMedDate not supplied

Distribution and expression of toxic shock syndrome toxin 1 gene among Staphylococcus aureus isolates of toxic shock syndrome and non-toxic shock syndrome origin.

Toxic shock syndrome toxin 1 (TSST-1), plays a significant role in the pathogenesis of TSS. TSST-1 production is subject to physiologic and environmental constraints. Thus, DNA probes that detect the chromosomal gene encoding the toxin are of value diagnostically, epidemiologically, and for studies of gene expression. Several synthetic oligonucleotide probes complementary to two regions of the TSST-1 gene were used to ascertain the presence of this gene in the chromosomal DNA of 261 strains of S. aureus from various TSS-related and non-TSS-related sources. Isolates were from clinically confirmed menstrual and nonmenstrual cases of TSS and from healthy vaginal carriers of S. aureus. Other strains tested included clinical non-TSS isolates and food poisoning-associated staphylococcal isolates. Detection of the TSST-1 gene by the labeled gene probes correlated in all but two cases with production of TSST-1. Ten Centers for Disease Control (CDC) strains that were isolated from TSS patients and did not produce TSST-1 were also examined, as were several strains of Staphylococcus epidermidis isolated from patients with suspected TSS. Neither group of strains possessed the TSST-1 gene. Finally, a 7-kilobase DNA restriction fragment of S. aureus containing the entire TSST-1 gene was transformed into Escherichia coli strains HB101 and DH5 alpha via a plasmid vector.

Bacterial Toxins↗
PubMed1997

Induction of ventricular fibrillation by T-wave field-shocks in the isolated perfused rabbit heart: role of nonuniform shock responses.

OBJECTIVES: Single electrical field shocks are able to induce ventricular fibrillation (VF) if applied during the vulnerable period. During this period, a shock can either prolong the action potential duration or induce a new action potential. Whether the occurrence of different shock responses contributes to the induction of VF has not been investigated directly in the intact heart. METHODS: In 12 isolated Langendorff-perfused rabbit hearts seven monophasic action potentials (MAPs) were recorded simultaneously during the application of 838 T-wave shocks. Post-shock repolarization was assessed by classifying the shock-induced response in each MAP recording either as a full action potential or an action potential prolongation. Heterogeneity of post-shock repolarization was defined if both response patterns were present in different MAP recordings at the same time. The heterogeneity of post-shock activation was measured as the dispersion of the post-shock activation time (PS-AT). The arrhythmogeneity of a shock was quantified as the number of rapid shock-induced repetitive responses. RESULTS: Shocks inducing nonuniform repolarization were associated with greater arrhythmogeneity than shocks inducing uniform repolarization (17.6 +/- 30.0 versus 1.6 +/- 1.1 shock-induced repetitive responses, p < 0.001). The severity of the induced arrhythmia increased gradually with increasing nonuniformity of repolarization (p < 0.01 for a 10% increase), being maximal when the shock initiated near equal numbers of both full action potentials and action potential prolongations. The induction of severe arrhythmias by T-wave shocks was also associated with a higher dispersion of PS-AT (29 +/- 14 ms for the induction of VF, 19 +/- 12 ms for non-sustained arrhythmia, and 12 +/- 8 ms for no arrhythmic response, all p < 0.001). For VF inducing shocks, an increase in shock strength towards the upper limit of vulnerability decreased the dispersion of PS-AT from 34 +/- 15 ms to 23 +/- 11 ms (p < 0.001). CONCLUSIONS: Nonuniform post-shock repolarization and dispersed post-shock activation contribute to the induction of VF by T-wave shocks. A decreasing dispersion of PS-AT towards higher shock strengths may contribute to the decreased or abolished inducibility by shocks above the upper limit of vulnerability.

Action Potentials↗
PubMed1997

Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia.

OBJECTIVES: To determine and compare the respective concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, soluble TNF receptors, nitrite/nitrate (NO2-/NO3-), and procalcitonin in the plasma of patients with septic shock, cardiogenic shock, and bacterial pneumonia without shock; and to assess the predictive value of these mediators in defining patients with septic shock. DESIGN: Cohort study, comparing normal volunteers (controls) and patients with septic shock, cardiogenic shock, and bacterial pneumonia. SETTING: A collaborative study among an intensive care unit, an emergency room, and three research laboratories. PATIENTS: Mediators were measured at various times in 15 patients with septic shock (during the shock phase and during the recovery phase), in seven patients with cardiogenic shock during the shock phase, and in seven patients with severe bacterial pneumonia on day 1 of admission. INTERVENTIONS: Blood samples were collected at various times during the course of the disease. MEASUREMENTS AND MAIN RESULTS: TNF-alpha values were highest in the acute phase of septic shock (53 to 131 pg/mL during septic shock), while patients with bacterial pneumonia had intermediate concentrations (32 pg/mL). TNF-alpha concentrations were normal in patients with cardiogenic shock. IL-6 concentrations were highest in patients with acute septic shock (85 to 385 pg/mL). However, in contrast to TNF-alpha concentrations, IL-6 concentrations were normal in patients with bacterial pneumonia and increased in patients with cardiogenic shock (78 pg/mL). Soluble TNF receptors were increased in all three groups vs. controls, with the highest increase in patients with septic shock. NO2-/NO3- concentrations were highest (72 to 140 mM) in patients with septic shock, and were < 40 mM in the other groups of patients. Procalcitonin concentrations were only markedly increased in patients with septic shock (72 to 135 ng/mL, compared with approximately 1 ng/mL in the three other groups). The best predictive value for septic shock was found to be the measurements of NO2-/NO3- and procalcitonin concentrations. CONCLUSIONS: These observations showed that increase of proinflammatory cytokines was a consequence of inflammation, not of shock. In this study comparing various shock and infectious states, measurements of NO2-/NO3- concentration and procalcitonin concentration represented the most suitable tests for defining patients with septic shock.

Adult↗
PubMed1998

Increased expression of HDJ-2 (heat shock protein 40) and heat shock protein 70 in biopsy specimens of transplanted human lungs.

BACKGROUND: Heat shock proteins are expressed during several forms of stress and inflammation. This study was done to determine whether the expression of heat shock protein HDJ-2 (heat shock protein 40), heat shock protein 60, and heat shock protein 70 are increased during rejection in human pulmonary allografts. METHODS: Thirty-five transbronchial biopsy specimens were obtained from adult lung transplant recipients. Histologic analysis and assessment of heat shock protein HDJ-2, heat shock protein 60, and heat shock protein 70 mRNA expression was performed. Total RNA was extracted, reverse transcribed, and amplified by polymerase chain reaction with oligonucleotide primers specific for the heat shock proteins. The identity of the amplified message was verified by Southern blot and slot blot analysis. RESULTS: The expression of heat shock protein HDJ-2 was significantly higher in samples from lung transplant recipients undergoing rejection when compared with recipients without rejection or infection. Heat shock protein 70 expression was also increased in rejection. Expression of heat shock protein 60 did not show any increase in recipients with no evidence of rejection and infection or transplant recipients with rejection or infection. Serial analysis of heat shock protein HDJ-2 and heat shock protein 70 obtained in biopsy specimens during and after rejection showed a decrease of heat shock protein HDJ-2 and heat shock protein 70 expression after resolution of lung rejection. CONCLUSION: Our data demonstrate that the expression of heat shock protein HDJ-2 and heat shock protein 70 increases during lung rejection. However, only heat shock protein HDJ-2 was able to differentiate between rejection and infection. Measurement of heat shock protein HDJ-2 in transbronchial biopsy specimens may assist in the differential diagnosis between rejection and infection in lung transplant recipients.

Carrier Proteins↗
PubMed1997

[Biological effects of interacting shock waves. A modeling study of the effects of interacting shock waves using erythrocyte hemolysis].

AIM: The effects of high-energy shock wave on tissues were discussed in literature. The shock wave sources which were used for experiments were developed for stone fragmentation. The side effects of the applicators are generally low. Increase of shock wave pressure induce bigger negative pressure amplitude and this may cause significantly bigger side effects. We used tow shock waves, with time interval of 5 microseconds. In our opinion, the first shock wave causes acoustic inhomogenity in shock wave focus and therefore second shock wave acts in a region with different acoustic parameters. The second shock wave may loss energy in the focus area by dissipation or absorption. We termed the coupled shock waves as "interacting shock waves". METHODS AND RESULTS: Hemolysis of erythrocytes was used for examination of biological toxicity. Shock wave pressure was 80 MPa, the ratio of positive to negative pressure of single shock waves is 30. For correlation we applied 50 and 100 single shock waves and 50 or 100 couples of two shock waves. Hemolysis after 50 simple shock waves was 4.28 times lower compared with hemolysis after the same number of coupled shock waves (interacting shock waves). CONCLUSION: After 50 couples of shock waves hemolysis is 2.14 times higher compared with 100 single shock waves. This result suggests that the hypothesis of some interaction existing between two shocks applied in a very short time interval make future study rightful.

Hemolysis↗